PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33860196-2 2021 The second-generation proteasome inhibitor carfilzomib is thought to be a substrate of P-glycoprotein whose efficacy may correlate with P-glycoprotein activity; however, research concerning the first-in-class proteasome inhibitor bortezomib is inconsistent. Bortezomib 230-240 ATP binding cassette subfamily B member 1 Homo sapiens 87-101 33668794-2 2021 The aim of our study is to assess the expression of previously described genes that may influence the resistance to bortezomib treatment at the mRNA level (ABCB1, CXCR4, MAF, MARCKS, POMP, PSMB5, RPL5, TXN, and XBP1) and prognosis of MM patients. Bortezomib 116-126 ATP binding cassette subfamily B member 1 Homo sapiens 156-161 28509582-7 2017 We reported herein that hypoxia-mediated resistance to carfilzomib and bortezomib in MM cells is due to P-gp activity and was reversed by tariquidar, a P-gp inhibitor. Bortezomib 71-81 ATP binding cassette subfamily B member 1 Homo sapiens 104-108 30365089-3 2019 The mechanistic studies confirmed that the enhancement of Snail1 expression in bortezomib-resistant MMCs directly upregulated transcription of the intracellular MDR1 gene to immediately develop multiple drug resistance mechanisms and inhibited P53 protein expression through the Snail1/hsa-miRNA-22-3p/P53 pathway to inhibit tumor cell apoptosis. Bortezomib 79-89 ATP binding cassette subfamily B member 1 Homo sapiens 161-165 30441975-8 2018 Further, significant associations between SNPs in MDR1 and outcome of MM were found in 110 MM patients that underwent bortezomib-based treatment. Bortezomib 118-128 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 29766327-13 2018 The resistant cell lines demonstrated less accumulation of intracellular doxorubicin, and were cross-resistant to other Pgp client drugs: bortezomib, doxorubicin, and paclitaxel, but not cisplatin. Bortezomib 138-148 ATP binding cassette subfamily B member 1 Homo sapiens 120-123 28509582-7 2017 We reported herein that hypoxia-mediated resistance to carfilzomib and bortezomib in MM cells is due to P-gp activity and was reversed by tariquidar, a P-gp inhibitor. Bortezomib 71-81 ATP binding cassette subfamily B member 1 Homo sapiens 152-156 27813130-7 2017 Additionally, when nicardipine, another P-gp inhibitor, was combined with bortezomib or carfilzomib, enhanced inhibition of MDA-MB-231 cell proliferation was observed. Bortezomib 74-84 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 25216523-9 2014 Expression of the multi-drug resistance gene ABCB1/MDR1 was decreased and acetylation of alpha-tubulin, a marker of microtubule stabilization, was increased following bortezomib treatment. Bortezomib 167-177 ATP binding cassette subfamily B member 1 Homo sapiens 45-50 25576094-0 2015 Preferential cytotoxicity of bortezomib toward highly malignant human liposarcoma cells via suppression of MDR1 expression and function. Bortezomib 29-39 ATP binding cassette subfamily B member 1 Homo sapiens 107-111 25576094-5 2015 Bortezomib inhibited MDR1 expression and function more effectively in SW872-S cells than in SW872 cells, indicating that the increased cytotoxicity relies on the degree of proteasome inhibition. Bortezomib 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 21-25 25576094-7 2015 These results show that bortezomib exhibits preferential cytotoxicity toward SW872-S cells possibly via highly expressed SERCA2-associated MDR1 suppression and suggest that bortezomib may serve as a potent agent for treating advanced liposarcoma. Bortezomib 24-34 ATP binding cassette subfamily B member 1 Homo sapiens 139-143 25576094-7 2015 These results show that bortezomib exhibits preferential cytotoxicity toward SW872-S cells possibly via highly expressed SERCA2-associated MDR1 suppression and suggest that bortezomib may serve as a potent agent for treating advanced liposarcoma. Bortezomib 173-183 ATP binding cassette subfamily B member 1 Homo sapiens 139-143 25477008-8 2015 Bortezomib efflux via P-glycoprotein was confirmed by demonstrating reduced sensitivity (IC50 11.6 vs. 2.8 ng/ml) and intracellular concentrations (-56.1%) in over-expressing cells compared to controls. Bortezomib 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 22-36 25590413-5 2015 We found that compared to the parental human uterus sarcoma cell line MES-SA cells, MES-SA/Dx5 cells highly expressed the ABCB1 was more resistant to MG132 and bortezomib, escaping the proteasome inhibitor-induced apoptosis pathway. Bortezomib 160-170 ATP binding cassette subfamily B member 1 Homo sapiens 122-127 28000886-8 2017 In conclusion, the miR-631/UbcH10/MDR1 pathway is closely associated with the development of BTZ resistance in myeloma cells, and the overexpression of miR-631 can significantly improve BTZ sensitivity in resistant myeloma cells. Bortezomib 93-96 ATP binding cassette subfamily B member 1 Homo sapiens 34-38 28000886-8 2017 In conclusion, the miR-631/UbcH10/MDR1 pathway is closely associated with the development of BTZ resistance in myeloma cells, and the overexpression of miR-631 can significantly improve BTZ sensitivity in resistant myeloma cells. Bortezomib 186-189 ATP binding cassette subfamily B member 1 Homo sapiens 34-38 25216523-9 2014 Expression of the multi-drug resistance gene ABCB1/MDR1 was decreased and acetylation of alpha-tubulin, a marker of microtubule stabilization, was increased following bortezomib treatment. Bortezomib 167-177 ATP binding cassette subfamily B member 1 Homo sapiens 51-55 22145750-9 2012 CONCLUSION: Bortezomib is a promising potential therapy for acute leukemia, especially mdr1 drug-resistant leukemia. Bortezomib 12-22 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 24899604-1 2014 OBJECTIVES: The aim of this study was to observe the effects of bortezomib (PS341) on the expression of NF-kappaB (nuclear factor-kappa B), IkappaB (inhibitor kB) and P-gp (P-glycoprotein) of K562 cells induced by daunorubicin (K562/DNR). Bortezomib 64-74 ATP binding cassette subfamily B member 1 Homo sapiens 167-171 24899604-1 2014 OBJECTIVES: The aim of this study was to observe the effects of bortezomib (PS341) on the expression of NF-kappaB (nuclear factor-kappa B), IkappaB (inhibitor kB) and P-gp (P-glycoprotein) of K562 cells induced by daunorubicin (K562/DNR). Bortezomib 64-74 ATP binding cassette subfamily B member 1 Homo sapiens 173-187 24899604-6 2014 When K562/DNR were cultured with bortezomib, the expressions of NF-kappaB and P-gp induced by DNR were significantly suppressed and this effcet increased with the increase of the concentration or the action time of bortezomib. Bortezomib 33-43 ATP binding cassette subfamily B member 1 Homo sapiens 78-82 24899604-6 2014 When K562/DNR were cultured with bortezomib, the expressions of NF-kappaB and P-gp induced by DNR were significantly suppressed and this effcet increased with the increase of the concentration or the action time of bortezomib. Bortezomib 215-225 ATP binding cassette subfamily B member 1 Homo sapiens 78-82 23589314-4 2013 Resistance to bortezomib is multifactorial and there are conflicting indications that cellular overexpression of P-gp may contribute to resistance agent. Bortezomib 14-24 ATP binding cassette subfamily B member 1 Homo sapiens 113-117 23589314-6 2013 METHODS: Cell lines with different P-gp expression levels were used to determine the relationship between bortezomib and P-gp. Bortezomib 106-116 ATP binding cassette subfamily B member 1 Homo sapiens 121-125 23589314-9 2013 RESULTS: In the present study, we show that bortezomib is a substrate for P-gp, but not for the other drug efflux transporters. Bortezomib 44-54 ATP binding cassette subfamily B member 1 Homo sapiens 74-78 23589314-10 2013 Bortezomib activity is affected by P-gp expression and conversely, the expression of P-gp affect bortezomib"s ability to act as a P-gp substrate. Bortezomib 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 35-39 23589314-10 2013 Bortezomib activity is affected by P-gp expression and conversely, the expression of P-gp affect bortezomib"s ability to act as a P-gp substrate. Bortezomib 97-107 ATP binding cassette subfamily B member 1 Homo sapiens 85-89 23589314-10 2013 Bortezomib activity is affected by P-gp expression and conversely, the expression of P-gp affect bortezomib"s ability to act as a P-gp substrate. Bortezomib 97-107 ATP binding cassette subfamily B member 1 Homo sapiens 85-89 23589314-12 2013 We also demonstrate that bortezomib directly affects the expression and function of P-gp. Bortezomib 25-35 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 23589314-13 2013 CONCLUSIONS: Our findings strongly support a role for P-gp in bortezomib resistance and, therefore, suggest that combination of a P-gp inhibitor and bortezomib in P-gp positive myeloma would be a reasonable treatment combination to extend efficacy of this important drug. Bortezomib 62-72 ATP binding cassette subfamily B member 1 Homo sapiens 54-58 23589314-13 2013 CONCLUSIONS: Our findings strongly support a role for P-gp in bortezomib resistance and, therefore, suggest that combination of a P-gp inhibitor and bortezomib in P-gp positive myeloma would be a reasonable treatment combination to extend efficacy of this important drug. Bortezomib 62-72 ATP binding cassette subfamily B member 1 Homo sapiens 130-134 23589314-13 2013 CONCLUSIONS: Our findings strongly support a role for P-gp in bortezomib resistance and, therefore, suggest that combination of a P-gp inhibitor and bortezomib in P-gp positive myeloma would be a reasonable treatment combination to extend efficacy of this important drug. Bortezomib 149-159 ATP binding cassette subfamily B member 1 Homo sapiens 54-58 22145750-1 2012 INTRODUCTION: To study the effect of bortezomib alone or in combination with daunorubicin (DNR) on an mdr1 single-factor drug-resistant leukemia cell line K562/MDR1, a multifactor-resistant cell line K562/A02, a drug-sensitive cell line K562, and primary cells from acute myeloid leukemia patients. Bortezomib 37-47 ATP binding cassette subfamily B member 1 Homo sapiens 102-106 22145750-1 2012 INTRODUCTION: To study the effect of bortezomib alone or in combination with daunorubicin (DNR) on an mdr1 single-factor drug-resistant leukemia cell line K562/MDR1, a multifactor-resistant cell line K562/A02, a drug-sensitive cell line K562, and primary cells from acute myeloid leukemia patients. Bortezomib 37-47 ATP binding cassette subfamily B member 1 Homo sapiens 160-164 22512091-0 2012 The proteasome inhibitor bortezomib reverses P-glycoprotein-mediated leukemia multi-drug resistance through the NF-kappaB pathway. Bortezomib 25-35 ATP binding cassette subfamily B member 1 Homo sapiens 45-59 22235146-6 2012 As for ATP-binding cassette transporter-mediated efflux, lymphoid CEM/VLB cells with P-glycoprotein (Pgp)/multidrug resistance 1 overexpression exhibited substantial resistance to carfilzomib (114-fold), ONX0912 (23-fold), and ONX0914 (162-fold), whereas less resistance to BTZ (4.5-fold) was observed. Bortezomib 274-277 ATP binding cassette subfamily B member 1 Homo sapiens 85-99 22512091-9 2012 The bortezomib reversed leukemic multi-drug resistance in a dose-dependent manner as the result of decreasing IkappaB degradation, thus preventing the translocation of NF-kappaB into the nucleus and leading the down-regulation of mdr1 and a reduction in P-gp expression. Bortezomib 4-14 ATP binding cassette subfamily B member 1 Homo sapiens 230-234 22512091-8 2012 Bortezomib decreased IkappaB degradation, decreased NF-kappaB and NF-kappaB p65 activity, reduced P-gp/mdr1 mRNA expression, and increased the intracellular DNR concentration in K562/DNR cells in vitro. Bortezomib 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 98-102 22512091-9 2012 The bortezomib reversed leukemic multi-drug resistance in a dose-dependent manner as the result of decreasing IkappaB degradation, thus preventing the translocation of NF-kappaB into the nucleus and leading the down-regulation of mdr1 and a reduction in P-gp expression. Bortezomib 4-14 ATP binding cassette subfamily B member 1 Homo sapiens 254-258 22512091-8 2012 Bortezomib decreased IkappaB degradation, decreased NF-kappaB and NF-kappaB p65 activity, reduced P-gp/mdr1 mRNA expression, and increased the intracellular DNR concentration in K562/DNR cells in vitro. Bortezomib 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 103-107 19254348-2 2010 We observed the effects of bortezomib on a P-glycoprotein (P-gp) positive leukemia line K562/A02. Bortezomib 27-37 ATP binding cassette subfamily B member 1 Homo sapiens 59-63 22082269-3 2011 We confirmed our previously discovered observation that bortezomib affects the expression of genes involved in the formation of MDR (ABCB1 gene, also known as MDR1, and ABCC1-MRP1), reducing the amount of their mRNA. Bortezomib 56-66 ATP binding cassette subfamily B member 1 Homo sapiens 133-138 22082269-3 2011 We confirmed our previously discovered observation that bortezomib affects the expression of genes involved in the formation of MDR (ABCB1 gene, also known as MDR1, and ABCC1-MRP1), reducing the amount of their mRNA. Bortezomib 56-66 ATP binding cassette subfamily B member 1 Homo sapiens 159-163 22082269-5 2011 It was also shown that bortezomib increased the amount of Akt kinase phosphorylated form in cell lines of malignant cells KB 8-5 and K 562/i-S9 that overexpressed ABCB1 transporter (Pgp), and did not affect the amount of activated Akt in the corresponding wild-type cells. Bortezomib 23-33 ATP binding cassette subfamily B member 1 Homo sapiens 163-168 20532504-7 2010 These findings suggest a potential role for MRP1 and MDR1 SNPs in modulating the long-term outcome of relapsed and/or refractory myeloma patients treated with PLD + bortezomib. Bortezomib 165-175 ATP binding cassette subfamily B member 1 Homo sapiens 53-57 20532504-0 2010 Polymorphisms in the multiple drug resistance protein 1 and in P-glycoprotein 1 are associated with time to event outcomes in patients with advanced multiple myeloma treated with bortezomib and pegylated liposomal doxorubicin. Bortezomib 179-189 ATP binding cassette subfamily B member 1 Homo sapiens 63-79 20532504-5 2010 MDR1/3435(C > T), which was in Hardy-Weinberg equilibrium, showed a trend of association with PFS (p = 0.0578), response rate (p = 0.0782) and TTP (p = 0.0923) in PLD + bortezomib patients, though no correlation was found in the bortezomib arm. Bortezomib 172-182 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 20532504-5 2010 MDR1/3435(C > T), which was in Hardy-Weinberg equilibrium, showed a trend of association with PFS (p = 0.0578), response rate (p = 0.0782) and TTP (p = 0.0923) in PLD + bortezomib patients, though no correlation was found in the bortezomib arm. Bortezomib 232-242 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 20532504-6 2010 In a recessive genetic model, MDR1/3435 T was significantly associated with a better TTP (p = 0.0405) and PFS (p = 0.0186) in PLD + bortezomib patients. Bortezomib 132-142 ATP binding cassette subfamily B member 1 Homo sapiens 30-34 19254348-2 2010 We observed the effects of bortezomib on a P-glycoprotein (P-gp) positive leukemia line K562/A02. Bortezomib 27-37 ATP binding cassette subfamily B member 1 Homo sapiens 43-57 19254348-3 2010 The results showed that bortezomib has significant effects on P-gp positive K562/A02 cells including cytotoxicity (48 h IC(50): 171.36 nM), induction of apoptosis (31.71 +/- 1.07% apoptotic cells after 24 h treatment at 100 nM), and inhibition of proteasome chymotrypsin-like activity (relative activity to untreated controls: 20.07 +/- 0.66% at 24 h with 10 nM bortezomib). Bortezomib 24-34 ATP binding cassette subfamily B member 1 Homo sapiens 62-66 34915026-12 2022 Inhibitors of ER-associated degradation (ERAD) (eeyarestatin I) and the proteasome (MG132, bortezomib) prevented ABCB1 loss induced by CerS2/6 downregulation. Bortezomib 91-101 ATP binding cassette subfamily B member 1 Homo sapiens 113-118 17662692-3 2007 We provide evidence that the proteasome-inhibitors Bortezomib and MLN273 are both substrates of MDR-1 by using knockdown of MDR-1 via a transposon-based vector system stably expressing siRNA against MDR-1 in MDR-1-overexpressing K562/Dox cells. Bortezomib 51-61 ATP binding cassette subfamily B member 1 Homo sapiens 96-101 17662692-3 2007 We provide evidence that the proteasome-inhibitors Bortezomib and MLN273 are both substrates of MDR-1 by using knockdown of MDR-1 via a transposon-based vector system stably expressing siRNA against MDR-1 in MDR-1-overexpressing K562/Dox cells. Bortezomib 51-61 ATP binding cassette subfamily B member 1 Homo sapiens 124-129 17662692-3 2007 We provide evidence that the proteasome-inhibitors Bortezomib and MLN273 are both substrates of MDR-1 by using knockdown of MDR-1 via a transposon-based vector system stably expressing siRNA against MDR-1 in MDR-1-overexpressing K562/Dox cells. Bortezomib 51-61 ATP binding cassette subfamily B member 1 Homo sapiens 124-129 17662692-3 2007 We provide evidence that the proteasome-inhibitors Bortezomib and MLN273 are both substrates of MDR-1 by using knockdown of MDR-1 via a transposon-based vector system stably expressing siRNA against MDR-1 in MDR-1-overexpressing K562/Dox cells. Bortezomib 51-61 ATP binding cassette subfamily B member 1 Homo sapiens 124-129 17662692-7 2007 Our report provides evidence that MLN273 and, to a lesser degree, Bortezomib are both MDR-1-substrates, which might be relevant for drug-resistance in cancer. Bortezomib 66-76 ATP binding cassette subfamily B member 1 Homo sapiens 86-91 17096161-4 2007 EXPERIMENTAL DESIGN: Bortezomib sensitivity of cell lines overexpressing P-glycoprotein, multidrug resistance protein-1, breast cancer resistance protein and lung resistance protein was studied in the presence and absence of established modulators of these transport proteins. Bortezomib 21-31 ATP binding cassette subfamily B member 1 Homo sapiens 73-87 17096161-6 2007 RESULTS: Of the MDR mechanisms studied, only P-glycoprotein conferred resistance to bortezomib, and resistance was only twofold. Bortezomib 84-94 ATP binding cassette subfamily B member 1 Homo sapiens 45-59